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Unit Four
Circulation
Right AtriumPulmonary Artery
Vena cava
Aorta
Pulmonary capillary
Right Ventricle
Left atriumLeft ventricle Pulmonary
vein
Systemiccapillary
The cardiovascular system consists of the heart and blood vessels
Tissue fluid circulation
Blood circulation Lymph circulation
(Power)
Cerebral fluid circulation
人体淋巴系统
人体脑室系统
人体脑脊液循环
The valves ensure one-way flow of the blood in the cardiovascular system
AV valves
Arterial valves
Venous valves
Lymphatic valves
Bicuspid valve (Mitral valve)
Tricuspid valve
Aorta semilunar valve
Pulmonary semilunar valve
The function of circulatory system
Transports materials throughout the body
Nutrients, water, gases (O2, CO2), hormones, etc
Keeps homeostasis of internal environment
Regulates body temperature
Endocrines
atrial diuretic peptide, vascular active substances
Cardiac Physiology
Excitation & conduction ( Electrical activity )
Pumping function (mechanic activity )
Chapter 9
Cardiac Electrophysiology
The importance of cardiac EP
1. Basis of cardiac contraction and pumping activity 2. Target of drugs
3. Arrhythmia: diagnosis, treatment
4. Research
Section 1
The electrical activity of the cardiomyocyte
Transmembrane potential of the cardiomyocyte
Resting potential:
varies with different cells
Maximal diastolic potential:
shown only in cells with
autorhythmicity
Types of the cardiomyocytes Fast response cells:
1. Contractile (working) cells: ventricular myocytes
atrial myocytes
2. Autorhythmic cells: His bundle, Purkinje fibers
Internodal pathways
Slow response cells:
1. Autorhythmic cells: pacemaker cells in sinus node,
atrial-nodal zone and nodal-His zone of the AV node
2. Non-autorhythmic cells: cells in AV nodal zone
atrial-nodal zone
nodal zone
nodal-His zone
His bundle
internodal pathways
AV node
The structure of AV node
心房肌
希氏束 浦氏纤维
心室肌
窦房结
房室结
1. Transmembrane potential of the cardiac working (contractile) cells
Resting potential:
80 90 mV, IK1 channel (Kir channel)
Action potential:
fast response, 4 phases
AP of atrial myocyte
AP of ventricular myocyte
Ionic basis of the AP of cardiac contractile cells
Phase 0 (depolarizing phase): INa
Phase 1 (fast repolarizing phase 1): Ito
Phase 2 (plateau phase): IK, ICal
Phase 3 (fast repolarizing phase 2) : IK, IK1
Phase 4 (resting potential): IK1, Na+ pump, etc
Figure 9-6 ICal in ventricular cell
Figure 9-7 IKr and IKs in dog ventricular cell
I Kr
I Ks
2. Diastolic depolarization in cardiac autorhythmic cells
Purkinje fiber:
If, IK
P cell in the sinus node:
If, ICaT, IKr
Ionic basis of the AP of Purkinje fibers Phases 0-3 : similar with contractile cell Phase 4 (diastolic depolarization): If, IK
Different names of If:Ih (hyperpolarization activated cation channel)Pacemaker current
Ionic basis of If:Na+ K+
Ionic basis of the pacemaker cell in sinus node Phases 0: ICal
Phase 3: IK
Phase 4: If, ICaT
A rightward shift of the curve
means a greater If at the same
membrane potential
Early afterdepolarization
Delayed afterdepolarization
Section 2
The electrical characteristics of the cardiomyocyte
Physiological characteristics of cardiomyocyte
Excitability (兴奋性) Conductivity (传导性) Autothythmicity (or pacemaker activity)
(自律性) Contractility (收缩性)
1. Excitability Factors that determine the excitability:
(1) Na+ (or Ca2+) channel properties: resting activation inactivation
excitable excitated non-excitable
ARP, ERP
(2) The distance between resting potential (maximal d
iastolic potential) and threshold potential
Periodic changes of the excitability of LV cardiomyocyte after excitation
absolute refractory period (ARP) (0-55mV)
effective refractory period (ERP) (0-60mV)
relative refractory period (RRP) (60-80mV)
supranormal period (SNP) (80-90mV)
Normal excitability (90mV)
Postrepolarization refractoriness
1. Normal: slow response cell, the recovery of ICal is slow, such that the membrane is still refractory after full repolarization.
2. Abnormal: myocardial infarction/reperfusion
PVC Compensatory pause
♣ Factors that affect the excitability
Ions: [K+]o: slight high [K+]o increases excitabilty serious high [K+]o decreases excitabilty low [K+]o increases excitabilty
[Ca2+]o: high [Ca2+]o slightly decreases excitabilty via affecting Na+ channel low [Ca2+]o increases excitabilty
pH: low extracellular pH (acidosis)
2. Autorhythmicity ( 自动节律性) Sinus node is the dominant pacemaker of the heart Sinus rhythm (窦性节律) Latent pacemaker ( 潜在起搏点) Ectopic pacemaker (异位起搏点)
Ways by which sinus node controls the heart:
Capture ( 抢先占领) Overdrive suppression ( 超速驱动抑制)
Factors that affect the autorhythmicity: Velocity of diastolic depolarization
Maximal diastolic potential
Threshold potential
Autonomic nerve control of the autorhythmicity: Sympathetic discharge increases the autorhythmicity
Vagal nerve discharge decreases the autorhythmicity
Key point
Question: Why cardiocyte has a very long APD?
Answer: To guarantee that the heart does not
tetanize ( 强直收缩,痉挛) , but excites an
d
contracts periodically.
3. Conductivity ( 传导性) The myocardium is a functional syncytium ( 机能合胞体) ,
the excitation can conduct directly between cardiac cells.
Conduction pathways
1. The conduction of excitation in the atrium Preferential pathway (inter-atrial pathway)
Inter-atrial contractile cell conduction
A-V block1st degree: A-V conduction slowing P-R interval prolongation 1:1 conduction
2nd degree: (1) PR interval gradual prolongation, then a QRS lost (2) 2:1 conduction, PR interval may not necessarily prolong
3rd degree: complete AV block, AV dissociation
2. The conduction of excitation in the ventricle
How to measure cardiac conduction?
1. Electrical mapping ( 标测技术) Multi-electrode array
2. Optical mapping
Voltage-sensitive dye
Apex
RV
LV
LAD
Sock Electrode Array (125 bipolar electrodes)
2D 3D
RV
LV
Apex
Early site
Isochronal map (Global Epicardium)
Apex
RV
LV
LAD
Sock electrode array
Global epicardial mapping of VT
3.2 cm
3.8
cm
Plague Electrode Array (480 bipolar electrodes)
Dog heart
Computerized Electrical Mapping showing the propagation of cardiac activation
B (3882) C (3902)
E (3942)
A (3867)
D (3917) F(fiber orientation)
Septum
RVRV
LV
G (1342)
A (1252)
H (1432)
B (1272)
D (1297) E (1307)
C (1292)
I(fiber orientation)
Septum
RV
LV
F (1322)
Conduction block, wavebreak, and the initiation of VF during rapid pacing
Cardiac Wedge Preparation
Mapping area
Epi
Early site
Optical Map (Transmural Section)
Endo
Optical mapping of the origin of ventricular automaticity
a. 0 ms b. 3 ms c. 8 ms d. 11 ms
PM
endo
1 cm
epie. 21 ms f. 51 ms g. 71 ms h. 91 ms
xy
300 ms
x
y
Section 3
Surface ECG
Normal human Surface ECG
P wave: Atrial (left and right) activation
Amplitude: <0.25mV; Duration: 0.08-0.11sec
P-R interval: Atrial activation time + A-V conduction time Duration: 0.12-0.20sec
QRS complex: ventricular depolarization
S-T segment: all the ventricular cells are activated. upward shift: downward shift:
T wave: ventricular repolarization
Ta wave (atrial T wave): atrial repolarization merged in QRS
Q-T interval: ventricular activation time (depol + repol)
U wave: mechanism and significance unkown
How surface ECG forms?
ECG leads(1)Bipolar limb leads (Standard leads): measure t
he potential difference between two points.
Lead I: left arm (+) —— right arm ( - )
Lead II: left leg (+) —— right arm ( - )
Lead III: left leg (+) —— left arm ( - )
If the three limbs of Einthoven‘s triangle (assumed to be equilateral) are broken apart, collapsed, and superimposed over the heart, then the positive electrode for lead I is said to be at zero degrees relative to the heart (along the horizontal axis) (see figure below). Similarly, the positive electrode for lead II will be +60º relative to the heart, and the positive electrode for lead III will be +120º relative to the heart. This new construction of the electrical axis is called the axial reference system. With this system, a wave of depolarization traveling at +60º produces the greatest positive deflection in lead II. A wave of depolarization oriented +90º relative to the heart produces equally positive deflections in both lead II and III. In this latter example, lead I shows no net deflection because the wave of depolarization is heading perpendicular to the 0º, or lead I, axis.
“ 爱氏三角”
(2) Unipolar limb leads The combination of the electrodes of left arm, right arm and left leg show roughly a zero potential, this point is called central reference point ( 中心电端)
Unipolar limb leads ( 单极肢体导联): measure the
true potential of a point on the body surface, include:
VR, VL, VF ( No more used ) Augmented Limb Leads (Unipolar) ( 加压单极肢体导 联) : 3 resistances are loaded, the central reference point
is “really” zero.
aVR, aVL, aVF
The axial reference system
The aVL lead is at -30º relative to the lead I axis; aVR is at -150º and aVF is at +90º. The six limb leads of the ECG record electrical activity along the frontal plane ( 冠状面 ) relative to the heart. Using the axial reference system and these six leads, it is simple to define the direction of an electrical vector at any given instant in time. If a wave of depolarization is spreading from right-to-left along the 0º axis, then lead I will show the greatest positive amplitude. If a wave of depolarization is moving from left-to-right at +150º, then aVL will show the greatest negative deflection, etc.
(3) Chest leads (Unipolar): V1-V6
These are six positive electrodes placed on the surface of the chest over the heart in order to record electrical activity in a plane perpendicular to the frontal plane (figure). A wave of depolarization traveling toward a particular electrode on the chest surface will elicit a positive deflection.
Cell polarizes at resting condition, no potential difference exits between different sites
Cell is depolarizing (activating), just like electric dipole( 电偶极子) movement. source sink
During cell depolarizing,Electrode at the negative side records a downward deflection,and an upward deflection, vice versa.
Membrane polarization hypothesis of ECG interpretation( ECG 形成的膜极化学说)
During cell repolarizing,The source is behind the sink, the electrodes record deflections in opposite directions vs depolarization.
The body acts as a conductor of the electrical currents generated by the heart, it is possible to place electrodes on the body surface and measure cardiac potentials.
By convention, a wave of depolarization heading toward the positive electrode is recorded as a positive voltage (upward deflection in the recording).
Volume Conductor Principles of ECG Interpretation( ECG 形成的容积导体原理)
Cardiac tissue at resting state
Cardiac tissue partially excited
What is volume conductor?If you put a cell ( 电池) into the center of a container filled with salt solution, the solution will be charged and become a volume conductor. The nearer a point away from the positive pole, the higher the potential is. The potential at a given point can be calculated by the equation:
V = E (cos /r2)
(V, voltage. E, electromotive force)
A B
r
V
Similarly, the body is a volume conductor, the heart is li
ke an Electric dipole ( 电偶极子 ) during activation. it is p
ossible to place electrodes on the body surface and measur
e cardiac potentials.
Vector ( 矢量,向量) is a physical variance which shows both
quantity (intensity or length) and direction, for example, the mecha
nical force, electrical current, etc.
The parallel quadrangle law of the resultant
( 合力的平行四边形法则)
Vectorcardiogram ( 向量心电图,心电向量图) depicts change
s in current vector length and direction at different times during the
cardiac cycle.
Sequence of ventricular depolarization and QRS complex
Sequence of myocardial activation and vector ring
Key point:The ECG recorded by each of the six limb leads is the
projection of the frontal vector ring on the respective
lead axis.
( 六个肢体导联所记录的心电图是额面向量环在各导联上的投影 )
Vector rings:
1. P vector ring
2. QRS vector ring
3. T vector ring
Normal QRS and T vector rings QRS and T vector rings in cardiac hypertrophy
What will happen if heart rate is too fast?
1. Decrease in cardiac output 2. Instability of cardiac electrophysiology, VF
3. Heart failure
Epicardiogram
HR 333 bpmVF
HR 200 bpmPeriodic
HR 300 bpmAlternance
Pacing Interval (ms)
CL-
PI
(ms)
300
250
220
200
190
180(VF)
Pac
ing
Int
erva
l (m
s)
301 297 303 300
207 172 205 176
VFA
B
500ms
Period doubling bifercation and chaos during rapid pacing
Period doubling bifurcation and chaos
Period-doubling bifurcation to chaos during rapid pacing
室颤
Pacing Interval ( ms )
△ Cycle Length
(ms)
Cycle Number
PCL 300ms PCL 190ms
PCL 170ms PCL 160ms, VF
规则模式(正常) ABAB 模式(交替)
ABCDABCD 模式 浑沌( chaos )
CL(ms)
心率加快时出现的激动周期倍增和 VF 的诱发
室速向室颤转化时的倍周期分岔和浑沌现象
1. 规则心跳 ( 心率 200 BPM)
2. 交替节律 (ABAB 模式) ( 心率 300 BPM)
3. ABCDABCD 模式 ( 心率 316 BPM)
4. 浑沌 (chaos), 室颤
激动周期
( 心率 333 BPM)
0 2 4 6 8 10 12 14 16 18
160
180
200
220
240
A
0 2 4 6 8 10 12 14 16 18
240
250
260
240
220
210D
0 2 4 6 8 10 12 14 16 18
160
200
180
220
260
140
240
0 2 4 6 8 10 12 14 16 18120
140
160
180
200
220
C
0 2 4 6 8 10 12 14 16 18
220
200
180
160
140
120FE
0 2 4 6 8 10 12 14 16 18
260
240
220
200B
210
230
250
270
Cycle #
Act
ivat
ion
Cyc
le L
engt
h (m
s)Variety of phase-4 bifurcation of RR interval
PI 300ms PI 250ms PI 220ms
PI 200ms PI 180ms
VF
传导速度 (CV)
连续心跳
Conduction velocity alternans and VF during rapid pacing
CV period-doubling and VF during rapid pacing
Cycle #
Con
duct
ion
Tim
e (m
s)
VF
PI (ms)
Number of Cycle Length
300
200
190
#15 #16 #17 #18
180(VF)
15
-1515
15-15
-15-10
-50
CL-PI (ms)
心率逐渐加快时 CL 的时间和空间交替及 VF 的形成
100.0
-100.0
15.0
-15.0
8.0
-8.0
5.0
-5.0
1.0
-1.0A
Jinmin Cao, FIG.1
(VF)180 ms
185 ms
190 ms
200 ms
BCL=300 ms1.0
-1.0
5.0
-5.0
8.0
-8.0
15.0
-15.0
100.0
-100.0
300
200
190
185
180(VF)
PI(ms) CL-PI (ms)
#1 #2 #3 #4
Number of Cycle Length
心率逐渐加快时 CL 的时间和空间交替及 VF 的形成 (计算机模拟)
The first captured beat
300
200
190
180
170
160
PI (ms)
VF
1000 ms
R wave oscillation and VF during rapid pacing
DiastoIic Interval (ms)
APD (ms)
0 50 100 150 200 250 300 350 400
140
160
180
200
220
240
Y =-3.3617 + 41.4293 * LN(X)
APD restitution curve
Slope=1
0 50 100 150 200
0.3
0.4
0.5
CV
(m
/s)
舒张期 (ms)
APD restitution curve :决定激动的时间不均一性
CV restitution curve :决定激动的空间不均一性
0 50 100 150 200
50
100
150
200
AP
D (
ms)
舒张期 (ms)
斜率 <1
0 50 100 150 200
0.3
0.4
0.5
CV
(m
/s)
舒张期 (ms)
斜率 <1
0 40 80 120 160 200
50
100
150
200
AP
D (
ms)
舒张期 (ms)
斜率 >1
斜率 >1
致室颤
致室颤
抗室颤
抗室颤
Pacing Interval (ms)
CL-
PI
(ms)
VF
600500
400
300 280240
350
220
190
PI
260
450550
050100150200250300350400
160
140
180
200
220
240
DI (ms)
ERP (ms)
G (1342)
A (1252)
H (1432)
B (1272)
D (1297) E (1307)
C (1292)
I(fiber orientation)
Septum
RV
LV
F (1322)
心率很快时出现的传导阻滞、激动波阵面分裂和 VF
PI 300 ms
#16 #17 #19#18
PI 160 msInduction of VF
#2#1 #3 #4
Beat No.
#6#5 #7 (VF) #8 (VF)
A. Isochronal maps during pacingActivation Time (ms)
B. Electrograms
C. Iso-deviation maps of CL
PI 160 msInduction of VF
Cycle Length Variation (activation CL-PI, ms)
#1 #2 #3 #4Cycle No. #5 #6 #7 #8
Captured Beats
1 2 3 4 5 6VF
1 2 3 4 5 6 7 8
Pacing artifacts
VF
1 2 3 4 5 6 7 8VF
Captured Beats